Cortisol is higher in parkinsonism and associated with gait deficit

Charlett, André; Rj, Dobbs; Ag, Purkiss; Dj, Wright; Dw, Peterson; Weller, C.; Sm, Dobbs

doi:10.1111/j.1600-0404.1998.tb00614.x

Cited by 83 publications

(60 citation statements)

References 43 publications

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“…Our hypothesis is indirectly supported by previous reports showing that cortisol levels were significantly higher in PD patients compared to healthy controls and that cortisol concentrations significantly decreased after levodopa intake, particularly in patients with a more advanced stage of PD [7,8]. In fact, it has been demonstrated that PD patients lose weight throughout the progression of the disease [9].…”

Section: Tablesupporting

confidence: 78%

Decrease in Blood Cortisol Corresponds to Weight Gain following Deep Brain Stimulation of the Subthalamic Nucleus in Parkinson’s Disease

Růžička

Nováková²,

Jech³

et al. 2012

Stereotact Funct Neurosurg

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Section: Tablesupporting

confidence: 78%

Decrease in Blood Cortisol Corresponds to Weight Gain following Deep Brain Stimulation of the Subthalamic Nucleus in Parkinson’s Disease

Růžička

Nováková²,

Jech³

et al. 2012

Stereotact Funct Neurosurg

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“…This makes these areas more susceptible to the effects of stress in both human [27] and rat [28,29] . This is also observed in PD patients with a positive association between cortisol and gait deficits [30] . Several studies discuss how the stress may deteriorate the symptoms of PD patients.…”

supporting

confidence: 48%

Stress and Inflammation: A Detrimental Combination in the Development of Neurodegenerative Disease.

Pablos

Espinosa-Oliva

Sarmiento

et al. 2014

Inflamm Cell Signal

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Chronic stress accelerates the appearance of some neurodegenerative disorders, such as Alzheimer's disease and Parkinson´s disease. On this review we firstly, describe some human epidemiological studies that highlight the possibility that chronic stress could increase the incidence or the rate of incidence of Alzheimer's disease and Parkinson´s disease. Secondly, we discuss the important role of inflammation in the progression and development of these neurodegenerative diseases. Finally, we try to justify the relationship between stress and inflammation with some experimental data. This work strongly suggests that chronic stress could be considered a key factor for the development of neurodegenerative diseases through microglial activation. Keywords: stress; inflammation; neurodegenerative diseasesTo cite this article: Rocío M. de Pablos, et al. Stress and inflammation: a detrimental combination in the development of neurodegenerative disease. Inflamm Cell Signal 2014; 1: e182. doi: 10.14800/ics.182.Copyright: © 2014 The Authors. Licensed under a Creative Commons Attribution 4.0 International License which allows users including authors of articles to copy and redistribute the material in any medium or format, in addition to remix, transform, and build upon the material for any purpose, even commercially, as long as the author and original source are properly cited or credited. IntroductionStress could be simply defined as any disruption of homeostasis, whereas 'stressor' would be any of the myriads of internal or external challenges that cause this disruption [1][2][3][4] . Disturbed homeostasis initiates a series of events called the stress response or cascade; this wellchoreographed response will involve the hypothalamic pituitary adrenal (HPA) axis that is in charge to restore homeostasis. Stress is a condition of human experience and an important factor in the onset of various diseases [5] . In general, it is considered that stress is not reduced only to the dramatic stressful events in our lives but rather to all those little daily problems that are capable of raising the activity of physiological systems sufficiently to cause a wear.Exposure to stressful situations triggers the activation of two systems: the sympatho-adreno-medullary system and the HPA system [6] . The first leads to raise the levels of circulating adrenaline whereas the second run the release of corticosteroid hormones from the adrenal cortex. Corticosteroid hormones have the ability to cross the blood brain barrier owing to their lipophilic properties and 2014; 1: e182. doi: 10.14800/ics.182; © 2014 by Rocío M. de Pablos, et al. http://www.smartscitech.com/index.php/ics Page 2 of 8 interact with to two classes of receptors: mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) [7] . MR and GR have different affinity for corticosterone, whilst MR have great affinity GR show less attraction with the endogenous hormone. They also differ in their distribution; MR are located mainly within limbic regions (eg. amygdala and h...

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“…24 Also colonic specimens of PD patients show downregulation of occluding. 95 Objective measures of PD include leukocyte subset counts, 106 serum cortisol, TNF-a, 107,108 in addition to global motor scores in the peripheral blood mononuclear cell production of cytokines, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) expression. 109 An increase IL-6 concentration in blood collected four years earlier predicts PD in patients.…”

Section: Current Biomarkers and Investigational Techniques Usedmentioning

confidence: 99%

Gut Microbiota Dysfunction as Reliable Non-invasive Early Diagnostic Biomarkers in the Pathophysiology of Parkinson's Disease: A Critical Review

Nair

Ramachandran

Joghee

et al. 2018

J Neurogastroenterol Motil

119

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Recent investigations suggest that gut microbiota affects the brain activity through the microbiota-gut-brain axis under both physiological and pathological disease conditions like Parkinson’s disease. Further dopamine synthesis in the brain is induced by dopamine producing enzymes that are controlled by gut microbiota via the microbiota-gut-brain axis. Also alpha synuclein deposition and the associated neurodegeneration in the enteric nervous system that increase intestinal permeability, oxidative stress, and local inflammation, accounts for constipation in Parkinson’s disease patients. The trigger that causes blood brain barrier leakage, immune cell activation and inflammation, and ultimately neuroinflammation in the central nervous system is believed to be due to the chronic low-grade inflammation in the gut. The non-motor symptoms that appear years before motor symptoms could be reliable early biomarkers, if they could be correlated with the established and reliable neuroimaging techniques or behavioral indices. The future directions should therefore, focus on the exploration of newer investigational techniques to identify these reliable early biomarkers and define the specific gut microbes that contribute to the development of Parkinson’s disease. This ultimately should pave the way to safer and novel therapeutic approaches that avoid the complications of the drugs delivered today to the brain of Parkinson’s disease patients.

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Cortisol is higher in parkinsonism and associated with gait deficit

Cited by 83 publications

References 43 publications

Decrease in Blood Cortisol Corresponds to Weight Gain following Deep Brain Stimulation of the Subthalamic Nucleus in Parkinson’s Disease

Decrease in Blood Cortisol Corresponds to Weight Gain following Deep Brain Stimulation of the Subthalamic Nucleus in Parkinson’s Disease

Stress and Inflammation: A Detrimental Combination in the Development of Neurodegenerative Disease.

Gut Microbiota Dysfunction as Reliable Non-invasive Early Diagnostic Biomarkers in the Pathophysiology of Parkinson's Disease: A Critical Review

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